VP22 of Herpes Simplex Virus 1 Promotes Protein Synthesis at Late Times in Infection and Accumulation of a Subset of Viral mRNAs at Early Times in Infection
VP22 of Herpes Simplex Virus 1 Promotes Protein Synthesis at Late Times in Infection and Accumulation of a Subset of Viral mRNAs at Early Times in Infection
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DOI：
10.1128/jvi.02245-07
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发表时间：
2009-01-15
影响因子：
5.4
通讯作者：
Baines, Joel D.
中科院分区：
文献类型：
--
作者：
Duffy, Carol;Mbong, Ekaette F.;Baines, Joel D.
VP22由UL49基因编码，是单纯疱疹病毒1型(HSV-1)被膜中含量最丰富的蛋白质之一。在目前的研究中，我们表明VP22是感染后期最佳蛋白质合成所必需的。具体地说，在没有VP22的情况下，病毒蛋白积累到野生型水平，直到感染后6小时。当时，在没有VP22的情况下，大多数病毒蛋白质的持续合成显著减少，而蛋白质的稳定性没有受到影响。在我们分析的单个蛋白中，VP22是合成晚期病毒蛋白GE和GD以及速效蛋白ICP0所必需的，但对速效蛋白ICP4或ICP27的积累没有明显的影响。此外，我们发现VP22是在感染早期(而不是晚期)将mRNAs子集积累到野生型水平所必需的。特别是，VP22的存在促进了GE和GDmRNAs的积累，直到感染后9h，但在感染后期没有明显的影响。此外，VP22在感染后的任何时间对ICP0基因的表达均无显著影响。因此，在U(L)49缺失病毒中观察到的蛋白质合成和mRNA型在感染过程中的时间和受影响的基因方面都是可分离的，并表明VP22在促进病毒蛋白质和mRNAs积累方面具有单独的作用。最后，我们发现VP22的S对蛋白质合成和基因积累的影响不依赖于编码VP22相互作用伙伴VP16和VHS的基因突变。
VP22, encoded by the UL49 gene, is one of the most abundant proteins of the herpes simplex virus 1 (HSV-1) tegument. In the present study we show VP22 is required for optimal protein synthesis at late times in infection. Specifically, in the absence of VP22, viral proteins accumulated to wild-type levels until similar to 6 h postinfection. At that time, ongoing synthesis of most viral proteins dramatically decreased in the absence of VP22, whereas protein stability was not affected. Of the individual proteins we assayed, VP22 was required for optimal synthesis of the late viral proteins gE and gD and the immediate-early protein ICP0 but did not have discernible effects on accumulation of the immediate-early proteins ICP4 or ICP27. In addition, we found VP22 is required for the accumulation of a subset of mRNAs to wild-type levels at early, but not late, times in infection. Specifically, the presence of VP22 enhanced the accumulation of gE and gD mRNAs until similar to 9 h postinfection, but it had no discernible effect at later times in infection. Also, VP22 did not significantly affect ICP0 mRNA at any time in infection. Thus, the protein synthesis and mRNA phenotypes observed with the U(L)49-null virus are separable with regard to both timing during infection and the genes affected and suggest separate roles for VP22 in enhancing the accumulation of viral proteins and mRNAs. Finally, we show that VP22's effects on protein synthesis and mRNA accumulation occur independently of mutations in genes encoding the VP22-interacting partners VP16 and vhs.